In these studies we investigated the involvement of SOCS proteins in regulating ocular inflammatory diseases of infectious or autoimmune etiology. We recently showed that SOCS3 deletion in T Lymphocytes suppresses the development of chronic ocular inflammation by up-regulating CTLA-4 and inducing the expansion of regulatory T cells. We also successfully treated uveitis in mice by topical administration of eye drops formulated with membrane-penetrating SOCS mimetics that specifically target the Janus kinases, JAK1 and JAK2. We continue to use transgenic rats that over-express SOCS1 in the retina and mice with targeted deletion of SOCS1 in the retina to further elucidate the role of SOCS1 and SOCS3 in ocular diseases.